A was transferred to the cardiac catheterization suite for angiography which showed no hemodynamically significant stenosis or evidence of disrupted plaque in any arteries. Return of spontaneous circulation was achieved. He had a second PEA arrest for which he received CPR and thrombolytic therapy for a presumptive diagnosis of STE myocardial infarction (MI). He was initially stabilized and a 12-lead electrocardiogram (ECG) was performed (Figure 1) that revealed ST elevations (STE) in leads V1–V3, Q waves in lead V2, and reciprocal ST depressions in lateral and inferior leads. He subsequently collapsed and had a pulseless electrical activity (PEA) cardiac arrest. A, a 68-year-old male with no prior medical history, called EMS after experiencing retrosternal chest pain and presyncope. The ECG remains one of the first and most widely used tools in many work-ups due to its convenience, availability, and cost. IntroductionĪcute pulmonary embolism (APE) has variable clinical manifestations and should always be on a differential for shortness of breath, chest pain, or syncope. In this case report, we discuss the underlying physiological mechanisms responsible and offer management suggestions for emergency department and critical care physicians to better expedite the treatment of APE mimicking acute coronary syndrome on ECG. To our knowledge, this is the first case report of an APE presenting with these ECG findings suggestive of myocardial ischemia. Acute pulmonary embolism (APE) has variable clinical presentations. He was treated for a pulmonary embolism and was discharged 5 days later. His ongoing metabolic acidosis and dependence on an intra-aortic balloon pump, despite adequate cardiac output, prompted a CT pulmonary angiogram which showed multiple segmental filling defects. No critical disease was found and his left ventriculogram showed normal contraction. Return of spontaneous circulation was achieved and he underwent a coronary angiogram. He received thrombolytic therapy for a presumptive diagnosis of ST elevation myocardial infarction.

An ECG prior to his arrest revealed ST elevations in leads V1–V3, Q waves in lead V2, and reciprocal ST depressions in the lateral and inferior leads. A 68-year-old male presented to the emergency department with retrosternal chest pain, presyncope, and then a pulseless electrical activity cardiac arrest.

Reciprocal changes ekg